New Insights into Cellular Inflammation and Regeneration

A special issue of Life (ISSN 2075-1729). This special issue belongs to the section "Physiology and Pathology".

Deadline for manuscript submissions: closed (31 August 2025) | Viewed by 1786

Special Issue Editor


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Guest Editor
Laboratory of Inflammation Research, School of Life Science, Handong Global University, Pohang 37554, Republic of Korea
Interests: innate immunity; inflammation; immunometabolism; cell migration; autoimmunity; immunopathology; skin immunity; renal immunity; antigen presentation; T cell activation; macrophages; dendritic cells
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Special Issue Information

Dear Colleagues,

It is becoming increasingly clear that inflammation plays a pivotal role in orchestrating the repair of damaged tissues, acting as both a trigger and regulator of regenerative processes. However, the dual nature of inflammation—as both a facilitator and potential inhibitor of regeneration—remains a significant focus of contemporary research. This Special Issue seeks to advance our understanding of this complex interplay and highlight novel therapeutic strategies that leverage inflammation to promote effective regeneration.

The topics of interest include the following:

  • Molecular and cellular mechanisms linking inflammation and regeneration;
  • The role of immune cells in regulating tissue repair;
  • Therapeutic interventions targeting inflammatory pathways to enhance regeneration;
  • Biomarkers for assessing inflammation–regeneration dynamics;
  • Innovations in regenerative medicine addressing inflammation-induced challenges.

We invite submissions of original research articles, comprehensive reviews, and methodological advances that address these topics and related areas. Contributions should provide new insights into the fundamental biology of inflammation and regeneration, as well as translational approaches with clinical relevance.

This Special Issue offers an opportunity to showcase cutting-edge research at the intersection of inflammation and regeneration, with the potential to inform future therapeutic developments.

Dr. Jea-Hyun Baek
Guest Editor

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Keywords

  • cellular inflammation
  • tissue regeneration
  • immune modulation
  • regenerative medicine
  • inflammatory pathways
  • immune cells and tissue repair
  • chronic inflammation
  • biomarkers of regeneration
  • immune-tissue crosstalk
  • wound healing
  • fibrosis and regeneration
  • inflammation resolution
  • tissue remodeling
  • regenerative microenvironment
  • inflammation-driven pathogenesis
  • translational immunology

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Published Papers (1 paper)

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Review

25 pages, 1727 KB  
Review
Macrophage Plasticity and Regulatory Networks During the Transition from Inflammation to Fibrosis in the Kidney
by Yehun Moon, Jintaek Hong, Jinwoo Chung and Jea-Hyun Baek
Life 2026, 16(1), 52; https://doi.org/10.3390/life16010052 - 29 Dec 2025
Viewed by 1362
Abstract
Kidney fibrosis represents the final common pathway of nearly all progressive renal diseases, linking acute kidney injury (AKI) and chronic kidney disease (CKD) through a maladaptive repair process. Regardless of etiology, persistent inflammation and excessive extracellular matrix (ECM) deposition drive irreversible structural distortion [...] Read more.
Kidney fibrosis represents the final common pathway of nearly all progressive renal diseases, linking acute kidney injury (AKI) and chronic kidney disease (CKD) through a maladaptive repair process. Regardless of etiology, persistent inflammation and excessive extracellular matrix (ECM) deposition drive irreversible structural distortion and functional decline in the kidney. Among cellular mediators, macrophages occupy a central role across the continuum from acute injury to fibrosis, orchestrating both tissue injury and repair through dynamic transitions between pro-inflammatory (M1) and pro-fibrotic (M2) states in response to local cues. Here, we synthesize macrophage-driven mechanisms of renal fibrosis, emphasizing recruitment, infiltration, and local proliferation mediated by chemokine–receptor networks and mechanosensitive ion channels. In addition, in this review paper, we provide an overview on the dual roles of macrophages in acute inflammation and chronic remodeling through key cytokine signaling pathways (TLR4/NF-κB, IL-4/STAT6, TGF-β/Smad, IL-10/STAT3), highlighting how metabolic reprogramming, mechanochemical feedback via Yes-associated protein (YAP)/transcriptional coactivator with PDZ-binding motif (TAZ) signaling, and epigenetic modulators collectively stabilize the fibrotic macrophage phenotype. Also, emerging insights into mitochondrial dysfunction, succinate–succinate receptor 1 (SUCNR1) signaling, and autophagy dysregulation reveal the metabolic basis of macrophage persistence in fibrotic kidneys. Understanding these multilayered regulatory circuits offers a framework for therapeutic strategies that selectively target macrophage-dependent fibrogenesis to halt the transition from acute injury to chronic renal failure. Full article
(This article belongs to the Special Issue New Insights into Cellular Inflammation and Regeneration)
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